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P3.184 Temporal evolution of resistance rates among clinical isolates of neisseria gonorrhoeae from são paulo, brazil
  1. Rafael Affini Martiins1,
  2. Roberto José Carvalho Da Silva2,
  3. Dandara Cassu-Corsi1,
  4. Carolina Silva Nodar,
  5. Roberta Alessandra Lima Bocalon2,
  6. Rodrigo Cayô1,
  7. André Mario Doi1,
  8. Ana Cristina Gales1,
  9. Antonio Carlos Campos Pignatari1
  1. 1Laboratório Especial de Microbiologia Clínica – LEMC/ALERTA, São Paulo – SP, Brazil
  2. 2Centro de Referência e Tratamento de Doenças Sexualmente Transmissíveis – CRT/AIDS Santa Cruz, São Paulo – SP, Brazil

Abstract

Introduction The emergence of antimicrobial resistance among N. gonorrhoeae isolates is a major concern worldwide. Although quinolones and macrolides are still recommended for empirical treatment of urethritis according to our national guidelines.The objective of this study was to evaluate the antimicrobial susceptibility profile of N. gonorrheae recovered from 2003 to 2015 from outpatients assisted at the Centro de Referência e Treinamento DST/AIDS-CRT Santa Cruz, São Paulo – SP.

Methods The identification was carried out by MALDI-TOF MS. The minimal inhibitory concentrations (MIC) for penicillin, ceftriaxone, ciprofloxacin and azithromycin were determined by agar dilution method and interpreted according to CLSI (2016) clinical breakpoints, except for azithromycin, which was interpreted using EUCAST (2016). The genetic relationship of isolates presenting reduced susceptibility to ciprofloxacin was evaluated by ERIC-PCR. Hydrolysis rates towards ceftazidime and cefotaxime were evaluated by mass spectrometry.

Results Among the 125 n. gonorrhoeae recovered, reduced susceptibilities to penicillin, ciprofloxacin, and azithromycin were observed for 89.6% (112/125), 22.3% (21/94), and 26.4% (33/125) of the isolates. Only one isolate was resistant to ceftriaxone, with MIC of 0.5 µg/mL. Reduced susceptibilities to penicillin, ciprofloxacin and azithromycin were already observed in 2003, and increased over the years, while resistance to ceftriaxone was only observed in 2006. The ceftriaxone-resistant isolate did not present detectable hydrolysis for ceftazidime and cefotaxime, suggesting that a no enzymatic mechanism was involved.

Conclusion Our data corroborates with other international series and pose in question the recommended syndromic treatment with quinolones and azithromycin. Our result suggests that ceftriaxone still remains a valuable therapeutic option for the empirical treatment of gonococcal infections in Brazil. Further analysis will be performed in order to better characterise the genetic relationship and the resistance mechanisms involved.

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